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10.4049/jimmunol.1300837 http://scihub22266oqcxt.onion/10.4049/jimmunol.1300837 C3981072!3981072!24634489     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2014 ; 192 (8): 3676-85 Nephropedia Template TP {{tp|p=24634489|t=2014. Distinct requirements for activation of NKT and NK cells during viral infection |pdf=|usr=}}{{24634489}} gab.com Text Distinct requirements for activation of NKT and NK cells during viral infection JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24634489 #FOAvip Natural killer (NK) cells are key regulators of innate defense against mouse cytomegalovirus (MCMV). Like NK cells, NKT cells also produce high levels of IFN? rapidly after MCMV infection. However, whether similar mechanisms govern activation of these two cell-types, and the significance of NKT cells for host resistance, remain unknown. Here we show that although both NKT and NK cells are activated via cytokines, their particular cytokine requirements differ significantly, in vitro and in vivo. IL-12 is required for NKT cell activation in vitro, but is not sufficient, while NK cells have the capacity to be activated more promiscuously in response to individual cytokines from innate cells. In line with these results, GM-CSF-derived DC activated only NK cells upon MCMV infection, consistent with their virtual lack of IL-12 production, while Flt3L-derived DC produced IL-12 and activated both NK and NKT. In vivo, NKT cell activation was abolished in IL-12?/? mice infected with MCMV, while NK cells were still activated. In turn, splenic NK cell activation was more IL-18 dependent. The differential requirements for IL-12 and IL-18 correlated with the levels of cytokine receptor expression by NK and NKT cells. Finally, mice lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral replication. Taken together, our results show that NKT and NK cells have differing requirements for cytokine-mediated activation and both can contribute non-redundantly to MCMV defense, revealing that these two innate lymphocyte subsets function together to fine-tune antiviral responses. Twit Text FOAVip Distinct requirements for activation of NKT and NK cells during viral infection ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24634489 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24634489 #FOAvip English Wikipedia <ref>{{Cite pmid|24634489}}</ref> Distinct requirements for activation of NKT and NK cells during viral infection #MMPMID24634489 Tyznik AJ; Verma S; Wang Q; Kronenberg M; Benedict CA J Immunol 2014[Apr]; 192 (8): 3676-85 PMID24634489show ga Natural killer (NK) cells are key regulators of innate defense against mouse cytomegalovirus (MCMV). Like NK cells, NKT cells also produce high levels of IFN? rapidly after MCMV infection. However, whether similar mechanisms govern activation of these two cell-types, and the significance of NKT cells for host resistance, remain unknown. Here we show that although both NKT and NK cells are activated via cytokines, their particular cytokine requirements differ significantly, in vitro and in vivo. IL-12 is required for NKT cell activation in vitro, but is not sufficient, while NK cells have the capacity to be activated more promiscuously in response to individual cytokines from innate cells. In line with these results, GM-CSF-derived DC activated only NK cells upon MCMV infection, consistent with their virtual lack of IL-12 production, while Flt3L-derived DC produced IL-12 and activated both NK and NKT. In vivo, NKT cell activation was abolished in IL-12?/? mice infected with MCMV, while NK cells were still activated. In turn, splenic NK cell activation was more IL-18 dependent. The differential requirements for IL-12 and IL-18 correlated with the levels of cytokine receptor expression by NK and NKT cells. Finally, mice lacking NKT cells showed reduced control of MCMV, and depleting NK cells further enhanced viral replication. Taken together, our results show that NKT and NK cells have differing requirements for cytokine-mediated activation and both can contribute non-redundantly to MCMV defense, revealing that these two innate lymphocyte subsets function together to fine-tune antiviral responses. äDistinct requirements for activation of NKT and NK cells during viral (epmc).pdf DeepDyve Pubget Overpricing